The study's lead researcher is Riyi Shi, a medical doctor and professor of neuroscience and biomedical engineering in Purdue University's Department of Basic Medical Sciences, School of Veterinary Medicine, Center for Paralysis Research and Weldon School of Biomedical Engineering. Shi and his team of researchers have found that a certain environmental toxin could be held partially responsible for causing multiple sclerosis (MS).

The toxin, acrolein, is found in air pollutants like auto exhaust and tobacco smoke. It is also created inside the body when nerve cells are damaged.

Nerve cells are insulated with myelin, and when a person has MS, the myelin is dismantled and the nerve fibers are damaged. Researchers believe acrolein is responsible for the dismantling of the myelin as well as inducing the creation of free radicals, which are compounds that cause further injury to tissues that are already damaged due to trauma or disease.

"Only recently have researchers started to understand the details about what acrolein does to the human body," said Shi. "We are studying its effects on the central nervous system, both in trauma and degenerative diseases such as multiple sclerosis."

To see if the researchers were correct about acrolein's effects, Shi and his team of researchers used a disease much like MS to elevate the acrolein in the spinal cord tissues of mice by nearly 60 percent.

To neutralize acrolein and temporarily halt the onset of MS, Shi used the drug hydralazine, which is an FDA-approved medication normally used to treat hypertension. Previous studies conducted by Shi and his team have shown that hydralazine prevents acrolein from causing neuronal death.

For this particular study, researchers concluded that a connection existed between acrolein and MS because the elevated acrolein levels within the mice were reduced by 50 percent when given hydralazine. According to Shi, this study is the first concrete laboratory evidence showing a link between acrolein and MS.

"The treatment did not cause any serious side effects in the mice," said Shi. "The dosage we used for hydralazine in animals is several times lower than the standard dosing for oral hydralazine in human pediatric patients. Therefore, considering the effectiveness of hydralazine at binding acrolein at such low concentrations, we expect that our study will lead to the development of new neuroprotective therapies for MS that could be rapidly translated into the clinic."

In addition, the researchers have also discovered the specific chemical signature of hydralazine, which could lead to synthetic alternatives with less side effects.